Role of nitric oxide in ischemia-evoked release of norepinephrine from rat cortex slices.
- Author:
Kee Won KIM
1
;
Young Ah EUN
;
Dong Chan KIM
;
Kyu Park CHO
Author Information
1. Department of Pharmacology, Chonbuk National University, Chonju 561-180, South Korea.
- Publication Type:Original Article
- Keywords:
Cerebral ischemia;
Norepinephrine release;
Nitric Oxide
- MeSH:
Animals;
Brain;
Brain Ischemia;
Cerebrospinal Fluid;
Glucose;
Glutamic Acid;
Guanylate Cyclase;
Ischemia;
Methylene Blue;
Neurotransmitter Agents;
NG-Nitroarginine Methyl Ester;
Nitric Oxide Synthase;
Nitric Oxide*;
Norepinephrine*;
omega-N-Methylarginine;
Oxygen;
Rats*;
Receptors, N-Methyl-D-Aspartate;
S-Nitroso-N-Acetylpenicillamine;
Synaptic Transmission
- From:The Korean Journal of Physiology and Pharmacology
1997;1(6):673-679
- CountryRepublic of Korea
- Language:English
-
Abstract:
It has been generally accepted that glutamate mediates the ischemic brain damage, excitotoxicity, and induces release of neurotransmitters, including norepinephrine (NE), in ischemic milieu. In the present study, the role of nitric oxide (NO) in the ischemia-induced (3H)norepinephrine((3H)NE) release from cortex slices of the rat was examined. Ischemia, deprivation of oxygen and glucose from Mg2+/-free artificial cerebrospinal fluid, induced significant release of (3H)NE from cortex slices. This ischemia-induced (3H)NE release was significantly attenuated by glutamatergic neurotransmission modifiers. NG-nitro-L-arginine methyl ester (L-NAME), NG-monomethyl-L-arginine (L-NMMA) or 7-nitroindazole, nitric oxide synthase inhibitors attenuated the ischemia-evoked (3H)NE release. Hemoglobin, a NO chelator, and 5, 5-dimethyl-L-pyrroline-N-oxide (DMPO), an electron spin trap, inhibited (3H)NE release dose-dependently. Ischemia-evoked (3H)NE release was inhibited by methylene blue, a soluble guanylate cyclase inhibitor, and potentiated by 8-bromo-cGMP, a cell permeable cGMP analog, zaprinast, a cGMP phosphodiesterase inhibitor, and S-nitroso-N-acetylpenicillamine (SNAP), a nitric oxide generator. These results suggest that the ischemia-evoked (3H)NE release is mediated by NMDA receptors, and activation of NO system is involved.
